Pathology of the urinary system

Autoantibodies directed against the GBM

 

 

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results from formation of autoantibodies against the glomerular basement membrane (type II 

hypersensitivity reaction) → complement fixation → leukocyte infiltration; 

 

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this form of glomerulonephritis is important in humans but rare in domestic animals; 

 

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a typical example in humans is acute post-streptococcal GN: typically follows 1-2 weeks 

after a streptococcal throat infection; its pathogenesis is not yet completely understood: 

streptococcal antigens may become implanted in the glomeruli, or streptococcal bacteria may 

have altered the GBM, making it appear as foreign material to the body (there may also be a 

contribution from circulating Ag-Ab complexes, thus adding a type III hypersensitivity 

reaction to the disease). 

 

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auto-antibodies or immune-complex deposits activate complement in the glomerular capillaries or 

mesangium → fractions C3a, C5a and C567 are chemotactic for neutrophils and macrophages → 

phagocytic cells release proteolytic enzymes in the surrounding milieu which damage the basement 

membranes, capillaries or mesangium; interaction of complement fragments with platelets can also 

initiate coagulation and thrombosis; 

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immunosuppressive agents, antiinflammatory drugs and anticoagulants reduce injury in GN.